ArticleJournal of experimental & clinical cancer research : CR2026
Low expression of ALOX15B modulates immunosuppressive tumor microenvironment in diffuse large B-cell lymphoma via the TAP1/MHC-I axis.
Article in Journal of experimental & clinical cancer research : CR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
backgroundDiffuse large B-cell lymphoma (DLBCL) patients with 17p deletion (17p-) show variable outcomes under R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy. ALOX15B (arachidonate 15-lipoxygenase type B), located on chromosome 17p, regulates immune responses via arachidonic acid (AA) metabolism. This study investigates its role in DLBCL progression and explores its epigenetic regulation and therapeutic potential.
methodsWe analyzed bulk and single-cell transcriptomic data from DLBCL cohorts to evaluate ALOX15B expression and its correlation with clinical outcomes, immune microenvironment, and therapy resistance. Functional assays using siRNA knockdown, luciferase reporter, and drug sensitivity experiments were performed in DLBCL cell lines. Murine and patient-derived xenograft (PDX) models were employed to assess tumor behavior and treatment efficacy in vivo. Chromatin immunoprecipitation sequencing (ChIP-seq), assay for transposase-accessible chromatin using sequencing (ATAC-seq), were conducted to explore the epigenetic regulation of ALOX15B.
resultsLow ALOX15B expression was associated with inferior progression-free survival (PFS), immunosuppressive microenvironment, and reduced CD8 + T cell cytotoxicity in DLBCL. Mechanistically, ALOX15B deficiency led to upregulation of COX-2/PGE2 signaling and downregulation of the TAP1/MHC-I antigen presentation axis. Silencing ALOX15B promoted tumor cell proliferation and resistance to doxorubicin. Epigenetically, HDAC1/2 were enriched at the ALOX15B promoter region, repressing its expression. Treatment with the HDAC inhibitor tucidinostat restored ALOX15B expression, enhanced tumor cell apoptosis, reinstated antigen presentation, and reprogrammed the tumor immune landscape in both cell lines and in vivo models.
conclusionsALOX15B is a key epigenetically regulated gene in DLBCL that modulates the tumor immune microenvironment and response to chemotherapy. Its downregulation promotes immune evasion and treatment resistance, while tucidinostat effectively restores its expression and anti-tumor immunity. These findings highlight ALOX15B as a prognostic biomarker and therapeutic target, particularly in 17p− DLBCL.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.